Glucocorticoids have multiple effects on glucose metabolism, and glucose has been shown to be a precursor of lung phospholipids(2). It therefore seems possible that part of the mechanism by which glucocorticoids regulate lecithin synthesis in the fetal lung is through an alteration in carbohydrate metabolism. In this project, I would like to study this possible regulatory mechanism by determining how glucocorticoids affect glucose and glycogen metabolism and utilization, and how glucocorticoids affect other intermediary substrates and their utilization, with particular emphasis on fatty acids, glycerol, lactate, and acetate. Rabbit fetuses will be exposed to the glucocorticoid in utero, and at 27 days of gestation the fetal lungs will be studied using incubated lung slices. The prepartions will be incubated with radiolabeled glucose, glycerol, palmitate, linoleate, lactate, or acetate. After incubation, glycogen, glucose oxidation, lactate production, and the phospholipids will be measured. The incorporation of label into glycogen and the phospholipids will also be determined. Appropriate controls will be run. I hope that a better understanding of the role of glucocorticoids in regulating fetal lung surfactant synthesis will ultimately lead to the development of a safer and more specific drug for the induction of pulmonary surfactant production.